Abstract
Hemodialysis (HD) and peritoneal dialysis are associated with inflammatory events and immunological incompetence. The purpose of this study was to evaluate the effect of both uremia and dialysis modality on the production of cytokines and reactive oxygen species (ROS) by monocytes. four groups of subjects were studied: 28 chronic kidney disease (CKD) patients, 14 chronic HD patients, 14 patients on continuous ambulatory peritoneal dialysis (CAPD) patients, and 14 healthy volunteers. peripheral blood mononuclear cells (PBMC) were isolated from blood samples and incubated for 24 hr with or without lipopolysaccharide (LPS). TNF‐α and IL‐10 production by PBMC and serum levels of these cytokines were quantified by ELISA. Aliquots of whole blood were incubated in vitro and ROS production and phagocytosis were quantified by flow cytometry. Compared to the control group, Staphylococcus aureus–stimulated ROS production by monocytes was significantly lower in the HD group. The highest levels of unstimulated TNF‐α production in vitro were observed in the HD group. In the CKD group, as well as in the whole population, there were a negative correlation between TNF‐α production by unstimulated PBMC and ROS production by S. aureus–stimulated monocytes and a positive correlation between PMA‐stimulated ROS production by monocytes and unstimulated and LPS‐stimulated IL‐10 production by PBMC suggesting that the pro‐inflammatory state in CKD patients is associated with decreased response to infectious challenges.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.